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Binge Eating Disorder (BED) is a novel diagnostic entity characterized
by recurrent binge eating episodes without any of the subsequent
compensatory behaviour commonly seen in patients with bulimia (1).
Approximately 30% of patients participating in weight-loss programs
and 70% of individuals in Overeaters Anonymous display this condition
(2). Pharmacologic intervention may be an important part of a multidisciplinary
approach to treating binge eating behaviour. There are few studies
investigating pharmacologic treatments in cases of BED, but the
most studied group of agents are the selective serotonin reuptake
inhibitors (SSRIs) (3,4).
Topiramate is a broad-spectrum neurotherapeutic agent that has
been approved for use as an adjunctive therapy in the treatment
of partial-onset seizures in adults. Its mechanism of action is
not fully understood, but the drug is known to enhance g-amino butyric
acid (GABA) activity, to block voltage-dependent Na+ channels, to
antagonize kainate and AMPA glutamate receptors, and also to inhibit
carbonic anhydrase. Well-tolerated in clinical trials, topiramate’s
most common adverse effects are somnolence, dizziness, ataxia, speech
disorders, psychomotor slowing, and paresthesias. Additionally,
a retrospective review of epilepsy patients treated with topiramate
suggests that it may be associated with reduced appetite and weight
loss (5).
There is increasing interest in the use of topiramate to treat some
psychiatric disorders, and preliminary reports have already suggested
that topiramate may have mood-stabilizing properties in patients
with bipolar disorder (6,7). In the field of eating disorders, Shapira
and others published an open-label trial on topiramate use (100
to 1400 mg daily) in 13 patients with BED (8). In their study, all
patients had comorbid Axis I psychiatric disorders (bipolar or major
depressive disorder) and were receiving other psychotherapeutic
agents simultaneously. Eleven patients responded with a moderate-to-marked
reduction in binge eating frequency and associated weight loss.
Recently, we described the case of a morbidly obese woman with BED
and no neuropsychiatric comorbidity who had failed to respond to
other agents and was successfully treated with topiramate (9).
This study evaluates topiramate’s efficacy and tolerability
in obese patients with BED and in the absence of other psychiatric
DSM-IV Axis I comorbidity.
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Methods
We selected 8 consecutive female outpatients seeking treatment
for weight gain after they gave their informed consent. They fulfilled
the following inclusion criteria: a body mass index (BMI) above
30, the diagnosis of BED according to DSM-IV criteria, and at least
moderately severe binge eating behaviour, as expressed by a score
above 17 on the Binge Eating Scale (BES) . The exclusion criteria
included any comorbid DSM-IV Axis I psychiatric diagnosis, a history
of seizures or epilepsy, pregnancy, lactation, any kind of psychotherapy
within 3 months of entry to the study, clinically unstable medical
illness, clinically significant abnormal laboratory results, and
use of psychiatric medication or antiobesity agents within 3 months
of entry to the study. To diagnose BED and other associated psychiatric
conditions, we used the Structured Clinical Interview for DSM-IV
Axis 1 Disorders (SCID 1/P) (10). We used the Binge Eating Scale
(BES) (11) to assess the severity of the binge eating behaviour
and the Beck Depression Inventory (BDI) (12) to evaluate the associated
depressive symptoms. The study was approved by the Institute of
Diabetes and Endocrinology of Rio de Janeiro Ethical Committee.
The dosage of topiramate was gradually increased in increments
of 25 mg every week from 25 mg twice daily in the first 2 weeks
to the target dosage of 75 mg twice daily at the end of the second
month of treatment. This dosage was maintained until the end of
the study.
The efficacy outcome measures were the number of days with binge
eating episodes per week (DBE), the BES scores, the BDI scores,
body weight, and adverse events. All variables were evaluated by
a psychiatrist and an endocrinologist at the outset of the trial,
at 2-week intervals in the first 2 months (visit 1, visit 2, visit
3, and visit 4), and thereafter at 4-week intervals until the fourth
month of treatment ( visit 5 and visit 6). Statistical analysis
included paired t-tests to assess changes in scores from pre- to
posttreatment. An intent-to-treat analysis was employed, with the
last available evaluation carried forward as endpoint
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